This SuperSeries is composed of the SubSeries listed below.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
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View SamplesToll-like receptors (TLRs) are key regulators of innate immune responses, and their dysregulation is observed in numerous inflammation-associated malignancies, including gastric cancer (GC). However, the identity of specific TLRs and their molecular targets which promote the pathogenesis of human GC is ill-defined. Here, we sought to determine the clinical utility of TLR2 in human GC. TLR2 mRNA and protein expression levels were elevated in 50% of GC patient tumors across multiple ethnicities. TLR2 was also widely expressed among human GC cell lines, and DNA microarray-based expression profiling was conducted on RNA from NUGC4 and AZ521 cells either non-stimulated or stimulated with a combination of 10g/ml Pam3Cys-Ser-(Lys)4 and FSL-1.
No associated publication
Cell line, Treatment
View SamplesWe hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in pre-immortal MEF cell lines in which Hic1 was inactivated compared to controls.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
No sample metadata fields
View SamplesWe hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in immortal MEF cell lines in which Hic1 or p53 was inactivated.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
No sample metadata fields
View SamplesIdentify genes like Ifit1 which are induced in L929 cells but not L929 cells expressing ectopic IRF8
Interferon Regulatory Factor 8 (IRF8) Impairs Induction of Interferon Induced with Tetratricopeptide Repeat Motif (IFIT) Gene Family Members.
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View SamplesIdentification of novel, highly penetrant, breast cancer susceptibility genes will require the application of additional strategies beyond that of traditional linkage and candidate gene approaches. Approximately one-third of inherited genetic diseases, including breast cancer susceptibility, are caused by frameshift or nonsense mutations that truncate the protein product [1]. Transcripts harbouring premature termination codons are selectively and rapidly degraded by the nonsense-mediated mRNA decay (NMD) pathway. Blocking the NMD pathway in any given cell will stabilise these mutant transcripts, which can then be detected using gene expression microarrays. This technique, known as gene identification by nonsense-mediated mRNA decay inhibition (GINI), has proved successful in identifying sporadic nonsense mutations involved in many different cancer types. However, the approach has not yet been applied to identify germline mutations involved in breast cancer. We therefore attempted to use GINI on lymphoblastoid cell lines (LCLs) from multiple-case, non-BRCA1/2 breast cancer families in order to identify additional high-risk breast cancer susceptibility genes.
No associated publication
Sex, Cell line
View Samples63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. The aim of this study was to identify potential downstream targets of key oncogenes and TSGs in melanoma (including p14ARF, p16INK4A, BRAF etc).
Confirmation of a BRAF mutation-associated gene expression signature in melanoma.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Enduring epigenetic landmarks define the cancer microenvironment.
Sex, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part, Treatment
View Samples35 Melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 microarrays were analysed for genes differentially expressed between cell lines carrying wild-type p14ARF and those with mutant 14ARF. All of these cell lines contained wild-type p53 (so that the effects of p14ARF mutations could be analysed without contamination from p53).
Gene expression profiling in melanoma identifies novel downstream effectors of p14ARF.
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